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1 ics into aberrant cells that overexpress the LDL receptor.
2  ultimately disrupt the interaction with the LDL receptor.
3 SK9 modulates atherosclerosis mainly via the LDL receptor.
4 e resident proteins and an ER-trapped mutant LDL receptor.
5 its role in promoting the degradation of the LDL receptor.
6 cretion is to some extent independent of the LDL receptor.
7 ic expression of SREBP-2 and its target, the LDL receptor.
8 red for clathrin-mediated endocytosis of the LDL receptor.
9 of apoE3-NT to interact with heparin and the LDL receptor.
10 erol levels by regulating the degradation of LDL receptors.
11 large VLDL, which are removed from plasma by LDL receptors.
12 ) receptor family, suggesting involvement of LDL receptors.
13 ch particles compared with mice lacking only LDL receptors.
14 teins by the liver and work independently of LDL receptors.
15  degradation of the low-density lipoprotein (LDL) receptor.
16 otein that degrades low-density lipoprotein (LDL) receptors.
17 elets via its receptor, lectin-like oxidized LDL receptor-1 (LOX-1), and alphabeta amyloid peptide, w
18 aken up by endothelial cells primarily by ox-LDL receptor-1 (LOX-1).
19 ing 15-lipoxygenase and lectin-type oxidized LDL receptor-1 both in vitro and in vivo.
20 ing factor receptor and lectin-like oxidized LDL receptor-1 to attenuate Akt activation and trigger g
21  Arg-164 in frizzled 1 domain and Arg-427 in LDL receptor 5 domain, respectively.
22 s that result in loss of function within the LDL receptor, a major determinant of inherited hyperlipi
23 hypercholesterolemia patients with defective LDL receptor activity but no reduction in those who were
24   SiRNA-depletion of Dab2 profoundly reduced LDL-receptor activity in ARH fibroblasts as a result of
25       Consistent with this, Pep2-8 inhibited LDL receptor and EGF(A) domain binding to PCSK9 with IC5
26 owed that placental LPL acts in concert with LDL receptor and LRP1.
27 ting furin-cleaved PCSK9 is able to regulate LDL receptor and serum cholesterol levels, although some
28 s should be the most effective in preserving LDL receptors and in lowering plasma LDL cholesterol.
29 oclonal antibody, increases the recycling of LDL receptors and reduces LDL cholesterol levels.
30 DL) receptors, increasing the degradation of LDL receptors and reducing the rate at which LDL cholest
31 ulating the hepatic low-density lipoprotein (LDL) receptors and increasing the clearance of LDL-chole
32  binding to hepatic low-density lipoprotein (LDL) receptors and promoting their lysosomal degradation
33 duced genes that promote cholesterol uptake (LDL receptor) and biosynthesis (HMG-CoA reductase).
34 pe 9) is a negative regulator of the hepatic LDL receptor, and clinical studies with PCSK9-inhibiting
35 one, with or without a genetic defect in the LDL receptor, and in subjects intolerant to statins, the
36 EBP-1c, SREBP-2, ChREBP, FATP1, HMGCoAR, and LDL receptor, and increasing Acox1 and ABCA1.
37 es involved in cholesterol biosynthesis, the LDL receptor, and PCSK9; a secreted protein that degrade
38 ced vitamin D deficiency in two backgrounds (LDL receptor- and ApoE-null mice) that resemble humans w
39 gainst the development of atherosclerosis in LDL-receptor/ApoB48-deficient mice.
40 rited disorder caused by mutations either in LDL receptor, apolipoprotein B (APOB), or proprotein con
41 amilial hypercholesterolaemia-causing genes, LDL receptor, apolipoprotein B and PCSK9, the most likel
42 tics and endocytosis of LDL particles by the LDL receptor are common in the general population and in
43  antibodies that inhibit its function on the LDL receptor are evaluated in phase III clinical trials.
44  and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inh
45 e start with a brief introduction to LDL and LDL receptor, as well as the advantages of using rLDL pa
46 In contrast, blocking LDL receptor with RAP (LDL receptor-associated protein) stopped the internaliza
47 ase PCSK9 binds the low-density lipoprotein (LDL) receptor at the surface of hepatocytes, thereby pre
48 ese results are consistent with increases in LDL receptors available to clear IDL and LDL from blood
49 (AT2 +/y) and deficient (AT2 -/y) mice in an LDL receptor -/- background were fed a saturated-fat enr
50                  Incubation with WT enhanced LDL receptor binding activity by 40% (+20% for GT and +0
51 , susceptibility to aggregation, LDL and non-LDL receptor-binding, and aortal deposition.
52 ies showed that MG(min)-LDL was bound by the LDL receptor but not by the scavenger receptor and had i
53 ycle, 4) LDL-induced aneuploidy requires the LDL receptor, but not Ass, showing that LDL works differ
54 esearch on a novel regulatory pathway of the LDL receptor by PCSK9, a new class of such drugs with a
55           The effect that blocking access to LDL receptors by VLDL, or internalisation of VLDL partic
56 protein (LDL) receptor family member, termed LDL receptor class A domain containing 3 (LRAD3), which
57      PCSK9 stimulates internalization of the LDL-receptor, decreases cholesterol uptake into hepatocy
58 s via DC-ASGPR, but not lectin-like oxidized-LDL receptor, Dectin-1, or DC-specific ICAM-3-grabbing n
59 d mice developed hyperlipidemia due to a non-LDL receptor defect in clearance of circulating apoB-con
60 ean+/-SD LDL cholesterol reductions in the 6 LDL receptor-defective patients were 19.3+/-16% and 26.3
61 ifferent populations including patients with LDL receptor defects (heterozygous familial hypercholest
62                Compounding the mutation with LDL receptor deficiency caused enhanced accumulation of
63 protective role in early lesion formation in LDL receptor deficient mice, and Crry-Ig and soluble C1
64                                              LDL receptor-deficient (Ldlr(-/-)) mice transplanted wit
65 by studying the effects of IgM deficiency in LDL receptor-deficient (Ldlr(-/-)) mice.
66 aliskiren over a broad dose range to fat-fed LDL receptor-deficient (Ldlr(-/-)) mice.
67                         Moreover, in fat-fed LDL receptor-deficient (Ldlr-/-) mice whose myeloid cell
68                             Western diet-fed LDL receptor-deficient (Ldlr-/-) mice with myeloid-speci
69  ABCG1 in T cells impacts atherosclerosis in LDL receptor-deficient (LDLR-deficient) mice, a model of
70 afb-deficient fetal liver cells in recipient LDL receptor-deficient hyperlipidemic mice revealed acce
71 tivity and activation of coagulation in both LDL receptor-deficient mice and African green monkeys.
72                                     Finally, LDL receptor-deficient mice expressing no (KO/L), normal
73 nistration of Slit2 to atherosclerosis-prone LDL receptor-deficient mice inhibited monocyte recruitme
74                          CAPN6 deficiency in LDL receptor-deficient mice restored CWC22/EJC/Rac1 sign
75                             Reversa mice are LDL receptor-deficient mice that develop atherosclerosis
76       PCPE2-deficient mice were crossed with LDL receptor-deficient mice to obtain LDLr(-/-), PCPE2(-
77                    Diabetic and non-diabetic LDL receptor-deficient mice were fed diets containing 0%
78                             Cholesterol-fed, LDL receptor-deficient mice were treated with either an
79 n these transgenic mice were crossed with an LDL receptor-deficient mouse model and were fed a high-f
80                         We therefore used an LDL receptor-deficient mouse model, in which type 1 diab
81 d-type (WT), apolipoprotein E-deficient, and LDL receptor-deficient mouse models.
82 n E (Apoe(-/-)) and low-density lipoprotein (LDL) receptor-deficient (LDLr(-/-)) mice.
83 ike 4 (Dll4) in atheromata and fat tissue in LDL-receptor-deficient mice.
84 exin type 9 (PCSK9) activity on cell-surface LDL receptor degradation.
85 regulation of LDL-cholesterol via control of LDL receptor degradation.
86 ithin:cholesterol acyltransferase (LCAT) and LDL receptor double knock-out mice (Ldlr(-/-)xLcat(-/-)
87  down-regulates the low-density lipoprotein (LDL) receptor, elevating LDL cholesterol and acceleratin
88 ions that work primarily via upregulation of LDL receptor expression (ie, diet, bile acid sequestrant
89 tatin therapies that act via upregulation of LDL receptor expression to reduce LDL-C were associated
90 creased LDL reuptake through upregulation of LDL receptor expression.
91 ipoproteins to leukocytes without changes in LDL-receptor expression.
92 e structures of LDL and its complex with the LDL receptor extracellular domain (LDL.LDLr) at extracel
93 omplement-type ligand binding repeats in the LDL receptor family are thought to mediate the interacti
94                                 Furthermore, LDL receptor family member antagonism with receptor-asso
95 general antagonist for binding of ligands to LDL receptor family members, inhibited APC-induced phosp
96 r affinity found for most protein ligands of LDL receptor family members.
97 e known to be critical for ligand binding to LDL receptor family receptors, relatively small reductio
98 interacting with an endogenous member of the LDL receptor family to have these effects.
99 receptor-related protein 1), a member of the LDL receptor family, acts as an endocytic receptor for B
100 nner that depends upon Lrp4, a member of the LDL receptor family, and muscle-specific kinase (MuSK),
101 hermore, we identified LRP1, a member of the LDL receptor family, as a new LeX carrier protein expres
102                        LDLR, a member of the LDL receptor family, binds to apoE, yet its potential ro
103  for trafficking of megalin, a member of the LDL receptor family, from EE to the ERC by coupling it t
104 e interaction with the largest member of the LDL receptor family, low-density lipoprotein receptor-re
105 d required the engagement of a member of the LDL receptor family.
106 or-related protein 1 (LRP1), a member of the LDL receptor family.
107 licated in driving the ligand binding to the LDL receptor family.
108  identified a novel low-density lipoprotein (LDL) receptor family member, termed LDL receptor class A
109 n antagonist of the low-density lipoprotein (LDL) receptor family, suggesting involvement of LDL rece
110 rs of RAP-dependent low-density lipoprotein (LDL) receptor family.
111 ubstantially raised LDL cholesterol, reduced LDL receptor function, xanthomas, and cardiovascular dis
112 antial reduction in low-density lipoprotein (LDL) receptor function, severely elevated LDL cholestero
113 taining mono- and biallelic mutations of the LDL receptor gene as models of familial hypercholesterol
114 or all members of the evolutionarily ancient LDL receptor gene family, is the major genetic modifier
115 ted prevalence of type 2 diabetes by APOB vs LDL receptor gene was 1.91% vs 1.33% (OR, 0.65 [95% CI,
116    Statins activate low-density lipoprotein (LDL) receptor gene expression, thus lowering plasma LDL
117      Members of the low-density lipoprotein (LDL) receptor gene family have a diverse set of biologic
118 c methods to evaluate the effect of diet and LDL receptor genotype on macrophage foam cell formation
119 e expression of the low-density lipoprotein (LDL) receptor homolog, LpR2.
120 or degradation via inducible degrader of the LDL receptor (IDOL) overexpression, using liver-targeted
121 diates posttranscriptional regulation of the LDL receptor in response to intracellular cholesterol le
122 lfate proteoglycans work in concert with the LDL receptor in the liver to facilitate binding and clea
123 f plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defin
124  and PCSK9; a secreted protein that degrades LDL receptors in the liver.
125  9 (PCSK9) binds to low-density lipoprotein (LDL) receptors, increasing the degradation of LDL recept
126  recognition process likely governs the ApoE-LDL receptor interaction.
127 e (LCAT) knock-out mice, particularly in the LDL receptor knock-out background, are hypersensitive to
128         We placed Ldlr(-/-) and heterozygous LDL receptor knockout (Ldlr(+/-)) mice on a high-cholest
129  native LDL, or ox-LDL and in hyperlipidemic LDL receptor knockout (LDLR(-/-)) mice that was effectiv
130 eloid alpha1AMPK knockout (MAKO) mice on the LDL receptor knockout (LDLRKO) background to investigate
131 8-deficient CD11c+ DCs into Western diet-fed LDL receptor knockout mice and found that the transplant
132                       Human AR expression in LDL receptor knockout mice exacerbates vascular disease,
133 FcgammaRIIB knockout (FcRIIB(-/-)) mice into LDL receptor knockout mice.
134 atherosclerotic lesion area was displayed in LDL receptor-KO mice transplanted with ERalpha(-/-) bone
135 mera containing the LDLa module of the human LDL receptor (LB2) demonstrated two key N-terminal regio
136                            Mice deficient in LDL receptor (Ldlr(-/-)) and mice lacking both TGH and L
137                     Induction of diabetes in LDL receptor (Ldlr(-/-)) knockout mice also leads to mar
138 3) or human apoE4 (E4) mice deficient in the LDL receptor (LDLR(-/-)).
139                            Mice lacking both LDL receptor (LDLR) and Arhgef1 were protected from high
140 lesterolemia because of its ability bind the LDL receptor (LDLR) and enhance its degradation in endos
141  cholesterol (LDL-C) by interacting with the LDL receptor (LDLR) and is an attractive therapeutic tar
142               Hepatic clearance involves the LDL receptor (LDLR) and possibly other receptors.
143 etary fatty acid composition on, lipoprotein-LDL receptor (LDLR) binding, and hepatocyte uptake, acco
144                             Mutations in the LDL receptor (LDLR) cause familial hypercholesterolemia
145                             The mechanism of LDL receptor (LDLR) degradation mediated by the proprote
146  importance of elevated circulating LDL, and LDL receptor (LDLR) expression in tumor cells, on the gr
147 ng of remnant lipoproteins to members of the LDL receptor (LDLR) family and cell-surface heparan sulf
148 at hnRNP K is specifically involved in human LDL receptor (LDLR) gene transcription in HepG2 cells.
149                         Lipid uptake via the LDL receptor (LDLR) has been shown for digalactosylceram
150                                          The LDL receptor (LDLR) mediates efficient endocytosis of VL
151  hypercholesterolemia is typically caused by LDL receptor (LDLR) mutations that result in elevated le
152 ent of LDL, is known to bind to cell surface LDL receptor (LDLR) or cell surface-bound proteoglycans
153                             LXR inhibits the LDL receptor (LDLR) pathway through transcriptional indu
154 L) is a recently identified regulator of the LDL receptor (LDLR) pathway.
155                                          The LDL receptor (LDLR) promotes post-translational degradat
156                        Here we show that the LDL receptor (LDLR) serves as the major entry port of VS
157              PCSK9 is a natural inhibitor of LDL receptor (LDLR) that binds the extracellular domain
158 sed by mutations in several genes, including LDL receptor (LDLR), apolipoprotein B (APOB), proprotein
159 d by variants in at least 3 different genes: LDL receptor (LDLR), apolipoprotein B-100, and proprotei
160     In humans and animals lacking functional LDL receptor (LDLR), LDL from plasma still readily trave
161 SK9 enhances the cellular degradation of the LDL receptor (LDLR), leading to increased plasma LDL cho
162  This multidomain protein interacts with the LDL receptor (LDLR), promoting receptor degradation.
163  cholesterol uptake receptors, including the LDL receptor (LDLR), the very LDLR, and the scavenger re
164 ible degrader of the LDL receptor) regulates LDL receptor (LDLR)-dependent cholesterol uptake, but it
165 wild type LRP6 (LRP6(WT)) and LRP6(R611C) in LDL receptor (LDLR)-mediated LDL uptake.
166 c target for hypercholesterolemia due to its LDL receptor (LDLR)-reducing activity.
167 eterozygote mutations R410S and G592E of the LDL receptor (LDLR).
168  after its cellular internalization with the LDL receptor (LDLR).
169  IDOL as a sterol-dependent regulator of the LDL receptor (LDLR).
170 olesterol from plasma to liver cells via the LDL receptor (LDLr).
171 evels by posttranslational regulation of the LDL receptor (LDLR).
172 rogenesis, we crossed mice deficient for the LDL receptor (Ldlr-/- mice) with mice that express low l
173  miR-33 inhibition in mice deficient for the LDL receptor (Ldlr-/- mice), with established atheroscle
174 g the endosomal and lysosomal degradation of LDL receptors (LDLR).
175 icking, such as the low-density lipoprotein (LDL) receptor (LDLR) and the ATP-binding cassette A1 (AB
176                 The low-density lipoprotein (LDL) receptor (LDLR) binds to and internalizes lipoprote
177 erosis by targeting low density lipoprotein (LDL) receptor (LDLR) degradation, this study investigate
178 9 (PCSK9) modulates low-density lipoprotein (LDL) receptor (LDLR) degradation, thus influencing serum
179 is interaction, the low-density lipoprotein (LDL) receptor (LDLR) has been proposed as a potential en
180 erexpression of the low density lipoprotein (LDL) receptor (LDLR) in HepG2 cells dramatically increas
181                 The low-density lipoprotein (LDL) receptor (LDLR) is a central determinant of circula
182 se bone marrow into low-density lipoprotein (LDL) receptor (LDLr) knockout mice (SMS2(-/-)-->LDLr(-/-
183 ough PCSK9 controls low density lipoprotein (LDL) receptor (LDLR) levels post-transcriptionally, seve
184                 The low density lipoprotein (LDL) receptor (LDLR) mediates efficient endocytosis of V
185 equence analysis of low-density lipoprotein (LDL) receptor (LDLR) mRNA did not reveal any amino acid
186  degradation of the low-density lipoprotein (LDL) receptor (LDLR), and its deficiency in humans resul
187 d the expression of low-density lipoprotein (LDL) receptor (LDLr), sterol regulatory element-binding
188 ve compounds on the low density lipoprotein (LDL) receptor (LDLR).
189 ven to mice lacking low density lipoprotein (LDL) receptors (Ldlr(-/-) mice).
190 ble degrader of the low-density lipoprotein [LDL] receptor [LDLR]) as a posttranscriptional regulator
191 ase subtilisin/kexin type 9 (PCSK9) binds to LDL receptors, leading to their degradation.
192 proteases, binds to low-density lipoprotein (LDL) receptors, leading to their accelerated degradation
193                       Moreover, they reduced LDL receptor levels in HepG2 cells and in mouse liver wi
194 ess of monoclonal antibodies that extend the LDL-receptor lifecycle (and thus result in substantial l
195                     The lectin-like oxidized LDL receptor LOX-1 mediates endothelial cell (EC) uptake
196 ytes in relation to the lectin-like oxidized LDL receptor (LOX-1).
197 alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of p
198 psin in the endoplasmic reticulum, deficient LDL receptor-mediated cholesterol uptake, and elevated l
199 possibility of a causal relationship between LDL receptor-mediated transmembrane cholesterol transpor
200 t and indisputably coexist, and both prevent LDL receptor-mediated uptake and promote macrophage scav
201 /kg/day) and AngII were co-infused into male LDL receptor -/- mice that were either AT2 +/y or -/y.
202                                         Male LDL receptor(-/-) mice were fed a saturated fat-enriched
203  dietary stimuli in low-density lipoprotein (LDL) receptor(-/-) mice.
204 at prevent interaction of PCSK9 with hepatic LDL receptors (monoclonal antibodies, mimetic peptides),
205                                    PCSK9 and LDL receptor mRNA levels in flash-frozen HCC and adjacen
206                                              LDL receptor mRNA was consistantly greater in HCC when c
207 e hepatic expression of apolipoprotein B and LDL receptor mRNAs with respect to the HF levels.
208                                      Type of LDL-receptor mutation, use of ezetimibe, coexistent diab
209  Patients with 2 defective versus 2 negative LDL receptor mutations had mean LDL-C reductions of 23.5
210 gene (APOB) mutations, and receptor-negative LDL receptor mutations were considered more severe than
211                     Low-density lipoprotein (LDL) receptor mutations were considered more severe than
212 se of the high prevalence of modestly severe LDL-receptor mutations in the Netherlands.
213                          Eight patients with LDL receptor-negative or -defective homozygous familial
214 t vascular smooth muscle cells isolated from LDL receptor null (Ldlr(-/-)) mice, which have impaired
215              Intravenous administration into LDL receptor null mice of targeted compared to non-targe
216 tein-restricted diet and 2) feeding C57BL/6J LDL receptor-null (LDLR(-/-)) dams a high-fat (Western)
217 , on lipid metabolism and atherosclerosis in LDL receptor-null (LDLRKO) mice.
218 xpansion were not significantly different in LDL receptor-null mice fed a saturated fat-enriched diet
219  potentially therapeutic protein can bind to LDL receptors on the BBB and be transcytosed into the CN
220                     These therapies increase LDL receptors on the cell surface and reduce plasma LDL
221 isulfide editing-dependent maturation of the LDL receptor or the reduction-dependent degradation of m
222 st to its previously reported effects on the LDL receptor, PCSK9 did not alter ENaC endocytosis or de
223         To achieve its maximal effect on the LDL receptor, PCSK9 requires autoproteolysis.
224  heparan sulfate proteoglycan (HSPG) and the LDL receptor, plus one docking receptor, SR-BI, signific
225  9 (PCSK9) binds to low-density lipoprotein (LDL) receptors, promoting their degradation and increasi
226 and activating a receptor complex containing LDL receptor protein 4 (Lrp4) and muscle-specific kinase
227       A significant 20% reduction in hepatic LDL receptor protein expression was also observed with e
228 ssion lowered plasma PCSK9 levels, increased LDL receptor protein expression, and restored plasma cho
229 llular levels with concomitant reductions of LDL receptor protein.
230                                 In contrast, LDL-receptor protein content was unchanged in Dab-2-depl
231           As well as the expected effects on LDL-receptor protein levels in the liver, mice expressin
232 oblasts as a result of profound reduction in LDL-receptor protein, but not mRNA; heterologous express
233 uitin ligase IDOL (inducible degrader of the LDL receptor) regulates LDL receptor (LDLR)-dependent ch
234 se subtilisin/kexin type-9 (PCSK9, a hepatic LDL-receptor regulator), inflammation, and adipose tissu
235 a consequence of the disruption of the PCSK9/LDL receptor regulatory axis.
236 of the TGF-beta-dependent signaling pathway: LDL receptor-related protein (LRP-1) and decorin.
237                                              LDL receptor-related protein (LRP1) is an endocytic and
238                                              LDL receptor-related protein (LRP1) is expressed by Schw
239 l surface stimulates association of CRT with LDL receptor-related protein (LRP1) to signal focal adhe
240 vity but required its membrane receptor, the LDL receptor-related protein 1 (LRP-1).
241 vity but required its membrane receptor, the LDL receptor-related protein 1 (LRP-1).
242 sing a haploid genetic screen, we identified LDL receptor-related protein 1 (LRP1) as a host cell rec
243                                              LDL receptor-related protein 1 (LRP1) is a highly modula
244                                          The LDL receptor-related protein 1 (LRP1) is a large endocyt
245                                          The LDL receptor-related protein 1 (LRP1) is a large endocyt
246           Recent studies have shown that the LDL receptor-related protein 1 (LRP1) is a physiological
247  rapid clearance of free Abeta40/42 from the LDL receptor-related protein 1 (LRP1) to the VLDL recept
248 epatic clearance of fVIII is mediated by the LDL receptor-related protein 1 (LRP1), a member of the L
249 ell biology techniques, we report that LRP1 (LDL receptor-related protein 1), a member of the LDL rec
250 igration through the surface receptor LRP-1 (LDL receptor-related protein 1)/CD91.
251 hat tPA induces Tyr(4507) phosphorylation of LDL receptor-related protein 1, which in turn leads to t
252 nterstitial fibroblast proliferation through LDL receptor-related protein 1-mediated beta1 integrin a
253 ndent of its protease activity, but required LDL receptor-related protein 1.
254 tion of the cytoplasmic tail of its receptor LDL receptor-related protein 1.
255  identified a contribution of the annexin A6/LDL receptor-related protein 1/thrombospondin 1 (ANXA6/L
256 bular protein extracts that we identified as LDL receptor-related protein 2 (LRP2), also known as meg
257 he closely related WNT signaling coreceptors LDL receptor-related protein 5 (LRP5) and LRP6 had redun
258               Mutation in the EGFP domain of LDL receptor-related protein 6 (LRP6(R611C)) is associat
259 y decreased expression of the Wnt coreceptor LDL receptor-related protein 6 (LRP6) in the mucosal tis
260 Loss-of-function mutations in Wnt coreceptor LDL receptor-related protein 6 (LRP6) underlie early-ons
261 f the frizzled (Fz) receptor, its coreceptor LDL receptor-related protein 6 (Lrp6), and the cytoplasm
262       We previously identified a mutation in LDL receptor-related protein 6 (LRP6), LRP6(R611C), that
263 that bind to the Frizzled (FZD) receptor and LDL receptor-related protein 6 (LRP6).
264      These effects required the WNT receptor LDL receptor-related protein 6 (LRP6).
265 ivation was determined by phosphorylation of LDL receptor-related protein 6, a coreceptor of Wnt liga
266 ular WNT activation by binding to the Kremen/LDL receptor-related protein receptors, was not seen wit
267 omposed of the receptor tyrosine kinase AXL, LDL receptor-related protein-1 (LRP-1), and RAN-binding
268 tective effect of tPA required its receptor, LDL receptor-related protein-1 (LRP-1).
269         Herein, we show that deletion of the LDL receptor-related protein-1 (LRP1) gene in Schwann ce
270                                              LDL receptor-related protein-1 (LRP1) is an endocytic an
271 death via an autocrine mechanism through the LDL receptor-related protein-1 (LRP1) receptor.
272   The endocytic and cell signaling receptor, LDL receptor-related protein-1 (LRP1), is reported to su
273 iption factor in SCs, unless counteracted by LDL receptor-related protein-1 (LRP1), which serves as a
274      Rapid ERK1/2 activation is dependent on LDL receptor-related protein-1 (LRP1).
275 rant peptide Angiopep-2 (An2), which targets LDL receptor-related protein-1 (LRP1).
276                                        LRP1 (LDL receptor-related protein-1) is a ubiquitous receptor
277 om type I collagen alpha chain, albumin, and LDL receptor-related protein.
278                                              LDL receptor-related proteins 5 and 6 (LRP5/6) are corec
279 tes express several Wnt receptors, including LDL receptor-related proteins 5 and 6, and Frizzled 1 to
280 ipoprotein E (ApoE) receptors, also known as LDL receptor-related proteins, have distinguished themse
281 of LTP across the Blood Brain Barrier by two LDL receptor-related proteins: LRP1 and Megalin.
282 nternalized through low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1) to become enzyma
283                     Low-density lipoprotein (LDL) receptor-related protein-1 (LRP1) has been shown to
284 is a ligand for the Low Density Lipoprotein (LDL) Receptor-related Protein-1 (LRP1), a multifunctiona
285                                              LDL-receptor-related protein 6 (LRP6), alongside Frizzle
286 structures of ligands in complex with tandem LDL receptor repeats or tandem CUB domains in other endo
287                  Additional studies with the LDL receptor showed a similar effect.
288 h that contacted by the EGF(A) domain of the LDL receptor, suggesting a competitive inhibition mechan
289 ed adaptor protein that sorts members of the LDL receptor superfamily (LDLR, megalin, LRP).
290                            It fully restored LDL receptor surface levels and LDL particle uptake in P
291 ertase subtilisin/kexin type 9 (PCSK9) binds LDL receptors, targeting them for degradation.
292                            In the absence of LDL receptors, the large VLDLs accumulate and produce ma
293 ession of PCSK9, a secreted inhibitor of the LDL receptor, thereby limiting their beneficial effects.
294 targets, and that inhibition of ACL leads to LDL receptor upregulation, decreased LDL-C and attenuati
295    To this end, the low-density lipoprotein (LDL) receptor was targeted for degradation via inducible
296 Thus, by inducing hepatic degradation of the LDL receptor, we generated a T2D model of combined kidne
297 ely target cancer cells that overexpress the LDL receptor while showing minor adverse impact on norma
298 oth furin- and hepsin-cleaved PCSK9 bound to LDL receptor with only 2-fold reduced affinity compared
299                        In contrast, blocking LDL receptor with RAP (LDL receptor-associated protein)
300  the role of AT(1a) receptors on leukocytes, LDL receptor(-/-)xAT(1a) receptor(+/+) or AT(1a) recepto

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